My laboratory studies molecular mechanisms that govern life-history plasticity, with a specific focus on aging. Unique plasticity in life-history progression, coupled with availability of genome sequence information, makes the honey bee (Apis mellifera) an ideal model for our research. Our work has established that aging in honey bees is better explained by behavioral role than by chronological age. This linkage is of particular interest because the natural behavioral progression of honey bees can be reversed. We have shown before that some aspects of honey bee aging, including immunosenescence and susceptibility to oxidative stress, are reversible along with behavior. Central to this plasticity is a regulatory pathway that incorporates a systemic hormone, juvenile hormone, and the gene vitellogenin, which encodes a major reproductive (yolk) protein precursor that is conserved between many taxa. Using RNA interference (RNAi), we have shown that vitellogenin controls several aspects of honey bee life-history; including social behavior by a suppressive effect on juvenile hormone, and including longevity by an ability to reduce oxidative stress. A link between social behavior and cellular aging through oxidative stress is particularly apparent in the honey bee brain, where damage accumulates at vastly different rates as a function of different social roles. The mechanistic basis for neuronal oxidative damage is under intense study because broader and improved knowledge can foster treatments for Alzheimer and Parkinson's disease. Oxidative damage increases irreversibly with age in the human brain, and similar progressive senescence is characteristic of the invertebrate- and vertebrate model species commonly used in aging research. Our work, however, suggests that this pattern need not be an absolute norm. Explicitly, neuronal aging may be a much more dynamic function of social behavior in honey bees. My lab aims to study this possibility in-depth, with the ultimate objective of developing a new neurogerontological model for research on oxidative stress induced damage in brain.